Читать книгу Respiratory Medicine - Stephen J. Bourke - Страница 101

‘Respiratory failure’ is a clinical term used to describe a failure to maintain oxygenation (usually taken as an arbitrary cut‐off point of PO₂ 8.0 kPa [60 mmHg]).

 Type I respiratory failure is hypoxaemia in the absence of hypercapnia. Overall alveolar ventilation is therefore normal. This pattern of abnormality usually indicates a disturbance of the V/Q matching system within the lung. Such a disturbance can be caused by any intrinsic lung disease affecting the airways, parenchyma or vasculature (e.g. acute asthma, lung fibrosis or pulmonary embolism).

 Type II respiratory failure is hypoxaemia with hypercapnia and indicates alveolar hypoventilation. Note this is not merely a severe form of type I respiratory failure; it is brought about by an entirely different mechanism. This may occur from reduced ventilatory drive (e.g. sedative overdose), reduced neuromuscular power (e.g. myopathy) or resetting of the chemoreceptors that drive ventilation in chronic lung disease (e.g. COPD).

Of course, type I and type II respiratory failure can coexist (and commonly do). These matters are dealt with in more detail in Chapter 1.

Oxygen saturation can be measured non‐invasively and continuously using a pulse oximeter. Oxygenated blood appears red, whereas reduced blood appears blue (clinical sign of cyanosis). An oximeter measures the ratio of oxygenated to total haemoglobin in arterial blood using a probe placed on a finger or earlobe, which comprises two light‐emitting diodes – one red and one infrared – and a detector. The light absorbed varies with each pulse, and measurement of light absorption at two points on the pulse wave allows the oxygen saturation of arterial blood to be determined. The accuracy of measurement is reduced if there is reduced arterial pulsation (e.g. low‐output cardiac states) or increased venous pulsation (e.g. tricuspid regurgitation, venous congestion). Skin pigmentation or the use of nail varnish may interfere with light transmission. Oximetry is also inaccurate in the presence of carboxyhaemoglobin (e.g. in carbon monoxide poisoning), which the oximeter detects as oxyhaemoglobin.

The relationship of PO₂ to oxygen saturation is described by the oxyhaemoglobin dissociation curve (see Fig . 1.9). This curve is sigma‐shaped, so that oxygen saturation is closely related to PO₂ only over a short range of about 3–7 kPa. Above this level, the dissociation curve begins to plateau and there is only a small increase in oxygen saturation as the PO₂ rises. Oximetry can reduce the need for arterial puncture, but arterial blood gas analysis is necessary to determine accurately the PO₂ on the plateau part of the oxyhaemoglobin dissociation curve, to measure CO₂ level and to assess acid/base status.